We have shown that intrathecal (i.t.) administration of etidronate (Eti) into mice produces an analgesic effect against the capsaicin-induced nociceptive behavior. However, the effect of Eti on neuropathic pain at the spinal level remains unknown. Therefore, we examined whether Eti attenuates pain after partial sciatic nerve ligation (PSNL). PSNL-induced tactile hyperalgesia observed on day 7 after the surgery was attenuated by oral and i.t. administration of Eti. The anti-hyperalgesic effect of i.t.-administered Eti was completely inhibited by an i.t. administration of ATP. The solute carrier family, SLC17, mediates the transport of pain transmitters, like ATP and glutamate. Indeed, we detected several members of the SLC17 family in the mouse dorsal lumbar spinal cord. Among the detected mRNAs, only Slc17a9, encoding for neuronal vesicular ATP transporter, was significantly increased upon PSNL. SLC17A9 protein levels were also significantly increased. In mice subjected to PSNL, SLC17A9 was present in neurons and microglia of the superficial dorsal horn. Collectively, our results suggest that Eti produces its anti-hyperalgesic effects by inhibiting SLC17A9-dependent exocytotic ATP release from the dorsal horn in mice subjected to PSNL.